中国组织工程研究 ›› 2026, Vol. 30 ›› Issue (33): 8794-8801.doi: 10.12307/2026.483

• 组织构建临床实践 clinical practice in tissue construction • 上一篇    下一篇

构建老年急性脑梗死患者出院时认知功能障碍的列线图预测模型与验证

高  琳,胡亦蓉,邓歆波,曾  瀛,熊  娟,施  欣   

  1. 宜春市人民医院神经内科,江西省宜春市   336000
  • 收稿日期:2025-11-13 修回日期:2026-03-16 出版日期:2026-11-28 发布日期:2026-06-17
  • 通讯作者: 胡亦蓉,宜春市人民医院神经内科,江西省宜春市 336000
  • 作者简介:高琳,女,1985年生,汉族,副主任医师,主要从事脑血管病及神经重症方面的研究。
  • 基金资助:
    江西省卫生计生委科技计划(20204734),项目负责人:胡亦蓉;江西省卫生健康委科技计划(202140869),项目负责人:高琳;江西省卫生健康委科技计划(202212643),项目参与人:高琳

Construction and validation of a nomogram prediction model for cognitive impairment at admission in elderly patients with acute cerebral infarction

Gao Lin, Hu Yirong, Deng Xinbo, Zeng Ying, Xiong Juan, Shi Xin   

  1. Department of Neurology, Yichun People’s Hospital, Yichun 336000, Jiangxi Province, China
  • Received:2025-11-13 Revised:2026-03-16 Online:2026-11-28 Published:2026-06-17
  • Contact: Hu Yirong, Department of Neurology, Yichun People’s Hospital, Yichun 336000, Jiangxi Province, China
  • About author:Gao Lin, Associate chief physician, Department of Neurology, Yichun People’s Hospital, Yichun 336000, Jiangxi Province, China
  • Supported by:
    Jiangxi Provincial Health and Family Planning Commission Science and Technology Program, No. 20204734 (to HYR); Jiangxi Provincial Health Commission Science and Technology Program, No. 202140869 (to GL); Jiangxi Provincial Health Commission Science and Technology Program, No. 202212643 (to GL [project participant]) 

摘要:



文题释义:
急性脑梗死:是一种因脑血管急性闭塞导致脑组织缺血缺氧的神经系统疾病。
认知功能障碍:指患者在脑梗死后出现的记忆、注意力、执行功能等认知能力减退。通过蒙特利尔认知评估量表进行诊断,评分< 26分(教育年限≤12年患者,评分< 25分)即判定为认知功能障碍。

背景:既往研究多聚焦于远期认知结局,尚缺少可在入院即刻基于血清生化指标量化老年急性脑梗死患者出院时认知功能障碍风险的工具。
目的:构建并验证基于入院时血清生化指标的预测模型,用以评估老年急性脑梗死患者出院时发生认知功能障碍的风险。
方法:前瞻性选择2023年7月至2024年6月期间在宜春市人民医院神经内科接受治疗的280例老年急性脑梗死患者,根据出院时是否发生认知功能障碍分为认知功能障碍组(n=157)和非认知功能障碍组(n=123)。另按照训练集与验证集7∶3的比例,选择2024年7月至2025年1月期间接受治疗的120例老年急性脑梗死患者为验证集。收集患者的临床及血清生化指标,通过单因素分析、最小绝对收缩和选择算子回归及多因素Logistic回归分析确定独立危险因素。采用Spearman相关性分析入院时血清生化指标与临床指标的关系。使用限制性立方样条模型分析入院时血清生化指标与认知功能障碍发生的非线性关系。将独立危险因素纳入Logistic模型中,构建血清生化指标模型及总预测模型,绘制列线图。通过受试者工作特征曲线下面积、混淆矩阵指标(准确率、精确率、召回率、F1分数)、校准曲线和决策曲线综合评估模型的预测效能、校准度及临床获益,并在验证集中进行验证。
结果与结论:400例患者认知功能障碍的发生率为55.0%。①确定11个老年急性脑梗死患者发生认知功能障碍的独立危险因素,分别为:年龄(OR=1.095,P < 0.001)、美国国立卫生研究院卒中量表评分(OR=1.121,P=0.013)、脑梗死部位(OR=1.785,P=0.006)、脑梗死类型(OR=1.587,P=0.017)、高血压(OR=2.200,P=0.014)、糖尿病(OR=2.249,P=0.011)、脑白质疏松(OR=2.031,P=0.022)、同型半胱氨酸(OR=1.088,P=0.020)、C-反应蛋白(OR=1.142,P=0.025)、高密度脂蛋白(OR=0.208,P=0.021)及25-羟基维生素D(OR=0.973,P=0.013);②Spearman相关性分析结果显示,老年急性脑梗死患者的同型半胱氨酸水平与脑梗死部位呈正相关(r=0.127,P < 0.05);C-反应蛋白水平与高血压、脑梗死类型呈正相关(r=0.259,P < 0.001;r=0.178,P < 0.001);高密度脂蛋白水平与年龄呈负相关(r=-0.131,P < 0.05);25-羟基维生素D水平与糖尿病呈负相关(r=-0.145,P < 0.05);③调整其他独立危险因素后,同型半胱氨酸和C-反应蛋白水平上升增加了认知功能障碍发生的风险,而高密度脂蛋白和25-羟基维生素D水平上升则降低了认知功能障碍发生的风险;④同型半胱氨酸、C-反应蛋白、高密度脂蛋白及25-羟基维生素D的风险临界值分别为21.44 μmol/L、11.73 mg/L、0.56 mmol/L、48.22 nmol/L;⑤血清生化指标模型在训练集和验证集的曲线下面积分别为0.852(0.809-0.895)和0.836(0.790-0.882),而总预测模型在训练集和验证集的曲线下面积分别为0.918(0.886-0.950)和0.895(0.857-0.933),且两个模型均展现出较好的预测效能、良好的校准度及临床获益。结果表明,基于入院时血清生化指标的列线图模型,对于老年急性脑梗死患者认知功能障碍发生风险具有良好的预测效能,可为临床早期识别认知功能障碍高危患者提供可视化工具。

https://orcid.org/0009-0004-7942-6860 (高琳) 


中国组织工程研究杂志出版内容重点:干细胞;骨髓干细胞;造血干细胞;脂肪干细胞;肿瘤干细胞;胚胎干细胞;脐带脐血干细胞;干细胞诱导;干细胞分化;组织工程

关键词: 血清生化指标, 脑梗死, 认知功能障碍, 危险因素, 列线图, 预测模型

Abstract: BACKGROUND: Previous studies have predominantly focused on long-term cognitive outcomes, and an instrument that can be applied immediately upon admission to quantify, based on serum biochemical markers, the risk of cognitive impairment at discharge in elderly patients with acute cerebral infarction is still lacking.
OBJECTIVE: To construct and validate a prediction model based on serum biochemical indicators at admission to evaluate the risk of cognitive impairment at discharge in elderly patients with acute cerebral infarction.
METHODS: A total of 280 elderly patients with acute cerebral infarction treated at the Department of Neurology, Yichun People’s Hospital from July 2023 to June 2024 were selected and divided into a cognitive impairment group (n=157) and a non-cognitive impairment group (n=123) based on the presence or absence of cognitive impairment at discharge. Another 120 patients treated from July 2024 to January 2025 were selected as the validation set in a 7:3 training-to-validation ratio. Clinical and serum biochemical indicators were collected. Independent risk factors were identified using univariate analysis, least absolute shrinkage and selection operator regression, and multivariate logistic regression. Spearman correlation analysis was used to assess the relationship between serum biochemical indicators at admission and clinical indicators. A restricted cubic spline model was employed to analyze the nonlinear relationship between serum biochemical indicators and cognitive impairment occurrence. Logistic models incorporating independent risk factors were constructed, and nomograms were developed. Model performance was comprehensively evaluated using the area under the area under the receiver operating characteristic curve (AUC), confusion matrix metrics (accuracy, precision, recall, and F1 score), calibration curves, and decision curves, with validation performed in the validation set.
RESULTS AND CONCLUSION: Among 400 patients, the incidence of cognitive impairment was 55.00%. (1) Eleven independent risk factors for cognitive impairment were identified: age (odds ratio [OR]=1.095, P < 0.001), National Institutes of Health Stroke Scale score (OR=1.121, P=0.013), cerebral infarction location (OR=1.785, P=0.006), cerebral infarction type (OR=1.587, P=0.017), hypertension (OR=2.200, P=0.014), diabetes (OR=2.249, P=0.011), leukoaraiosis (OR=2.031, P=0.022), homocysteine (OR=1.088, P=0.020), C-reactive protein (OR=1.142, P=0.025), high-density lipoprotein (OR=0.208, P=0.021), and 25-hydroxyvitamin D (OR=0.973, P=0.013). (2) The results of the Spearman correlation analysis showed that in elderly patients with acute cerebral infarction, the level of homocysteine was positively correlated with the location of cerebral infarction (r=0.127, P < 0.05); the level of C-reactive protein was positively correlated with hypertension and the type of cerebral infarction (r=0.259, P < 0.001; r=0.178, P < 0.001); the level of high-density lipoprotein was negatively correlated with age (r=-0.131, P < 0.05); and the level of 25-hydroxyvitamin D was negatively correlated with diabetes (r=-0.145, P < 0.05). (3) After adjusting for other independent risk factors, elevated homocysteine and C-reactive protein levels increased the risk of cognitive impairment, whereas increased levels of high-density lipoprotein and 25-hydroxyvitamin D decreased the risk of cognitive impairment. (4) Critical thresholds for homocysteine, C-reactive protein, high-density lipoprotein, and 25-hydroxyvitamin D were 21.44 μmol/L, 11.73 mg/L, 0.56 mmol/L, and 48.22 nmol/L, respectively. (5) The AUC values for the biochemical indicator model were 0.852 (0.809-0.895) in the training set and 0.836 (0.790-0.882) in the validation set, while those for the total prediction model were 0.918 (0.886-0.950) and 0.895 (0.857-0.933), respectively. Both models demonstrated good predictive performance, calibration, and clinical utility. These findings indicate that the nomogram model based on serum biochemical markers at hospital admission exhibits robust predictive power for the risk of cognitive impairment following ischemic stroke in elderly patients with acute cerebral infarction. It serves as a visual aid for the early clinical identification of patients at high risk for cognitive impairment.


Key words: serum biochemical indicators, cerebral infarction, cognitive impairment, risk factors, nomogram, prediction model

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